In the peanut (Arachis hypogaea L.) nonnodulation has been reported to be controlled by both duplicate recessive genes and a single recessive gene. In the present study genetics of peanut nonnodulation was investigated in four crosses from data on F₂ populations and F₃ progenies from nonnodulating F₂ plants. The F₂ data of all the four crosses studied showed a better fit for a trigenic ratio of 61 nodulating to three nonnodulating plants compared to the previously reported duplicate digenic ratio of 15 nodulating to one nonnodulating F, plants. Further, the segregation of F₂ progenies from nonnodulating F₂ plants indicated the inadequacy of the duplicate factor model. A new genetic model involving three genes in the inheritance of nonnodulation is proposed. Two genes produce nodulation while the third gene inhibits nodulation only when it is dominant and the former two genes are in recessive homozygous condition. By assuming differential heterozygosity at the three loci of the parents involved in various crosses, the duplicate factor and monogenic ratios reported by previous workers on nonnodulation could be explained by the new model. Although the occurrence or non-occurrence of nodules is governed by a few major genes, the intensity of nodulation appears to be controlled quantitatively. ICRISAT Journal Article no. 642.
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